The use of concurrent hormonotherapy and radiotherapy does not deteriorate radiation-induced cardiac toxicity

2016 ◽  
Vol 36 (8) ◽  
pp. 795-801 ◽  
Author(s):  
C Yavas ◽  
G Yavas ◽  
H Toy ◽  
O Ata

Postmenopausal patients with breast cancer have two options for adjuvant endocrine therapy, tamoxifen and aromatase inhibitors (AIs) as well as radiotherapy (RT) and chemotherapy. However, there is limited data regarding the optimal sequencing of RT and tamoxifen/AIs. Thus, we aimed to evaluate the effects of tamoxifen and AIs on radiation-induced cardiotoxicity. Eighty ovariectomized rats were divided into eight groups (G). G1 was defined as a control group; G2, G3, G4, and G5 were RT, tamoxifen, anastrozle, and letrozole groups, respectively; G6, G7, and G8 were RT plus tamoxifen, anastrozle, and letrozole groups, respectively. Drugs were started 1 week before RT and continued until the animals were killed 16 weeks after RT. The heart tissues were then dissected and examined with light microscopy to determine endocardial thickness and cardiac fibrosis. The endocardial thickness scores of both RT alone and the tamoxifen groups as well as the cardiac fibrosis score of RT alone were higher than that the control group ( p < 0.05 for all). There was no difference in the endocardial thickness and cardiac fibrosis scores of the RT-only group and the RT plus hormonotherapy groups ( p > 0.05 for all). Concurrent administration of RT and hormonal therapy with either tamoxifen or AIs did not further amplify radiation-induced cardiac toxicity. This issue warrants further study.

2020 ◽  
Vol 108 (3) ◽  
pp. e776-e777
Author(s):  
J.J. Meshman ◽  
D. Toomeh ◽  
L. Wang ◽  
S. Samuels ◽  
L.M. Freedman ◽  
...  

2010 ◽  
Vol 76 (3) ◽  
pp. 186-195 ◽  
Author(s):  
Nicolas Magné ◽  
Cyrus Chargari ◽  
Dhara MacDermed ◽  
Rosa Conforti ◽  
Lionel Védrine ◽  
...  

2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 758-758
Author(s):  
S. K. Das ◽  
A. Baydush ◽  
S. Zhou ◽  
M. Miften ◽  
X. Yu ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Rehab M. Elgharabawy ◽  
Ibrahim El Tantawy El Sayed ◽  
Nada Abd-Allah Rezk ◽  
Ehab Tousson

Breast cancer remains the most common cause of cancer deaths among women globally. Ehrlich solid tumor (EST) is a transplantable tumor model for simulating breast cancer. This study aims to describe the protective role of costus (Saussurea lappa) root against EST-induced cardiac toxicity. Forty female mice were randomly and equally divided into four groups (G1, control group; G2, costus group; G3, EST group; G4, EST + costus). The results showed that compared to the control, EST induced a significant increase in lactate dehydrogenase, creatine kinase, creatine kinase myoglobin, aspartate aminotransferase, and alkaline phosphatase activities; in potassium, chloride ion, cholesterol, triglyceride, and low density lipoprotein levels; in DNA damage and cardiac injury; and in p53 and vascular endothelial growth factor expression. Conversely, EST induced a significant decrease in sodium ion and high density lipoprotein levels and Ki67 expression compared to the control. Treatment of EST with costus improved cardiac toxicity, lipid profiles, electrolytes, and apoptosis, and protected against EST. This indicates the potential benefits of costus as an adjuvant in the prevention and treatment of cardiac toxicity.


2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Xuguang Hu ◽  
Dan Ding ◽  
Jiayi Zhang ◽  
Jianguo Cui

Abstract Radiotherapy is a major therapeutic strategy for breast cancer, while cancer radioresistance remains an obstacle for the successful control of the tumor. Novel radiosensitizing targets are to be developed to overcome radioresistance. Recently, long non-coding RNAs (lncRNAs) were proved to play critical roles in cancer progression. Among all, lncRNA HOTAIR was found to participate in cancer metastasis and chemoresistance. In the present study, we aimed to investigate the radiosensitizing effects of targeting HOTAIR and the underlying mechanism. Our data showed that HOTAIR (HOX antisense intergenic RNA) was up-regulated in breast cancer cells and tissues, and the expression of HOTAIR increased following irradiation. Knockdown of HOTAIR inhibited cell survival and increased cell apoptosis in response to ionizing radiation. Moreover, compared with control group, radiation induced more DNA damage and cell cycle arrest in HOTAIR knockdown cells. Finally, we found that the radiosentizing effects of HOTAIR were related to the up-regulation of miR-218, a ceRNA of HOTAIR. In conclusion, our finding showed that HOTAIR inhibition sensitizes breast cancer cells to ionizing radiation, induced severe DNA damage and activated apoptosis pathways, suggesting a possible role of HOTAIR as a novel target for breast cancer radiosensitization.


2018 ◽  
Vol 174 (1) ◽  
pp. 179-185 ◽  
Author(s):  
Mohamed Abouegylah ◽  
Lior Z. Braunstein ◽  
Mohamed A. Alm El-Din ◽  
Andrzej Niemierko ◽  
Laura Salama ◽  
...  

2004 ◽  
Vol 22 (14_suppl) ◽  
pp. 758-758
Author(s):  
S. K. Das ◽  
A. Baydush ◽  
S. Zhou ◽  
M. Miften ◽  
X. Yu ◽  
...  

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